Abstract
Melanogenesis is the biological process which the skin pigment melanin is synthesized to protect the skin against ultraviolet irradiation and other external stresses. Abnormal biology of melanocytes is closely associated with depigmented skin disorders such as vitiligo. In this study, we examined the effects of maclurin on melanogenesis and cytoprotection. Maclurin enhanced cellular tyrosinase activity as well as cellular melanin levels. We found that maclurin treatment increased the expression of microphthalmia-associated transcription factor (MITF), tyrosinase-related protein- (TRP-) 1, TRP-2, and tyrosinase. Mechanistically, maclurin promoted melanogenesis through cyclic adenosine monophosphate (cAMP) response element binding (CREB) protein-dependent upregulation of MITF. CREB activation was found to be mediated by p38 mitogen-activated protein kinase (MAPK) or cAMP-protein kinase A (PKA) signaling. In addition, maclurin-induced CREB phosphorylation was mediated through the activation of both the cAMP/PKA and the p38 MAPK signaling pathways. Maclurin-induced suppression of p44/42 MAPK activation also contributed to its melanogenic activity. Furthermore, maclurin showed protective effects against H2O2 treatment and UVB irradiation in human melanocytes. These findings indicate that the melanogenic effects of maclurin depend on increased MITF gene expression, which is mediated by the activation of both p38 MAPK/CREB and cAMP/PKA/CREB signaling. Our results thus suggest that maclurin could be useful as a protective agent against hypopigmented skin disorders.
Highlights
In recent years, an increase in fine dust caused by industrialization, abnormal climate change, and ozone layer destruction has created conditions that can cause damage to the human body, especially the skin
To examine the relationship between cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling and p38 Mitogen-activated protein kinases NF-κB (MAPKs) signaling in maclurin-induced melanogenesis, we examined the effects of H89 and SB203580 on cAMP-responsive element binding (CREB) phosphorylation levels
The results indicate that the melanogenic effects of maclurin occur mainly through microphthalmia-associated transcription factor (MITF) upregulation, which is mediated by two different signaling pathways, p38 MAPK and cAMP/PKA signaling
Summary
An increase in fine dust caused by industrialization, abnormal climate change, and ozone layer destruction has created conditions that can cause damage to the human body, especially the skin. To reduce the damage caused by external stress factors, the skin biosynthesizes melanin, a skin pigment. This process of skin pigment synthesis is called melanogenesis. Various stresses can cause defects in melanogenesis, leading to depigmentation skin ⁎ ⁎ ⁎. Oxidative Medicine and Cellular Longevity OH O HO OH. Melanin content (% of control) OH OH.
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